Renal servocontrol of arterial blood pressure.

Crawford, M. Pat; Richardson, Travis Q.; Guyton, Arthur C.

doi:10.1152/jappl.1967.22.1.139

Cited by 7 publications

(4 citation statements)

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“…Unfortunately the plasma sodium concentration was not measured in all the dogs of the present series. The pattern of such changes is in accordance with the results of Crawford et al (1967) who in the above-quoted paper demonstrated a statistically significant decrease of plasma sodium and chloride concentration during the development of arterial hypertension. A decrease of glomerular filtration per se, a direct effect of the angiotensin or an increase of vasopressin secretion, might all be responsible for an antidiuresis (Lever, 1965;Bock et al, 1968;Brown et al, 1969) with a possible expansion of plasma and extracellular volume independent of sodium retention.…”

Section: Haemodynamic Changessupporting

confidence: 89%

“…Gibson & Robinson (1938) found an increase of plasma volume in two out of four dogs 1-5 months after bilateral renal artery stenosis while in one dog plasma volume was substantially unchanged and in the last one it was decreased. On the other hand, Crawford, Richardson & Guyton (1967), by a gradual constriction of the renal artery to a lone remaining kidney in the conscious dog, provided indirect evidence of an expansion of extracellular volume during the increase of blood pressure.…”

Section: Haemodynamic Changesmentioning

confidence: 99%

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Effect in the Conscious Dog of Constriction of the Renal Artery to a Sole Remaining Kidney on Haemodynamics, Sodium Balance, Body Fluid Volumes, Plasma Renin Concentration and Pressor Responsiveness to Angiotensin

1970

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1.The renal artery to a lone remaining kidney was constricted in fourteen concious dogs. The following variables were measured in all animals: blood pressure (BP), cardiac rate (CR), plasma renin concentration (PRC), plasma volume (PV), extracellular fluid volume (ECFV) and plasma non-protein nitrogen (NPN). Sodium balance was estimated in eleven dogs. Cardiac output (CO), total peripheral resistence (TPR) and stroke volume (SV) were measured in nine dogs. Angiotensin responsiveness (AR) was measured in six animals.2. Within 2 hr the following changes occurred: a sharp increment of BP, PRC and TPR, with initial reduction or no change in CO and CR; SV and PV were not changed. The linear regression of BP changes on PRC changes did not differ statistically from the one previously obtained during the infusion of exogenous renin in the conscious dog. AR was much depressed at 2 hr.3. After 24 hr a slight but sigdicant sodium retention developed, while PV and ECFV and SV increased, CO remained unchanged owing to a decrease of CR. PRC tended to return toward normal while BP remained high. Thus the linear regression between these two variables disappeared. At this stage AR increased toward normal and in two dogs exceeded normal. 4.On days 3 4 and 6-7 after constriction, CO increased owing to a rise of SV, while TPR decreased. PV and ECFV were expanded while sodium balance was maintained. AR varied very much in the individual dogs according mainly to changes of PRC, sodium balance and PV. 5. On days 12-14 sodium balance became positive again, PRC returned within normal levels in almost all the dogs. PV and ECFV also tended to decrease to normal.CO and AR were measured in only two dogs at this stage.6. It is suggested that the early rise of blood pressure might be produced by the

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Section: Haemodynamic Changessupporting

confidence: 89%

Section: Haemodynamic Changesmentioning

confidence: 99%

Effect in the Conscious Dog of Constriction of the Renal Artery to a Sole Remaining Kidney on Haemodynamics, Sodium Balance, Body Fluid Volumes, Plasma Renin Concentration and Pressor Responsiveness to Angiotensin

1970

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“…Renal Na þ excretory function is intrinsically accountable for the long-term control of blood pressure [1,2]. A renal reduction in Na þ excretion, either by reduced glomerular filtration rate (GFR) or by increased tubular reabsorption of this electrolyte, causes hypertension.…”

Section: Introductionmentioning

confidence: 99%

How the Kidney Is Impacted by the Perinatal Maternal Environment to Develop Hypertension1

Paixão

Alexander

2013

Biology of Reproduction

120

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Environmental conditions during perinatal development such as maternal undernutrition, maternal glucocorticoids, placental insufficiency, and maternal sodium overload can program changes in renal Na(+) excretion leading to hypertension. Experimental studies indicate that fetal exposure to an adverse maternal environment may reduce glomerular filtration rate by decreasing the surface area of the glomerular capillaries. Moreover, fetal responses to environmental insults during early life that contribute to the development of hypertension may include increased expression of tubular apical or basolateral membrane Na(+) transporters and increased production of renal superoxide leading to enhanced Na(+) reabsorption. This review will address the role of these potential renal mechanisms in the fetal programming of hypertension in experimental models induced by maternal undernutrition, fetal exposure to glucocorticoids, placental insufficiency, and maternal sodium overload in the rat.

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“…First and foremost, there has been some debate as to whether the kidney is truly the controller of blood pressure as proposed by Crawford et al 4 some years ago. Although a detailed review of this debate is well beyond the scope of this commentary, most have concluded that the concepts developed by Guyton are applicable to a considerable portion of both experimental and human hypertension.…”

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confidence: 99%